Identification of 12 genetic loci associated with human healthspan.
Aleksandr A ZeninYakov A TsepilovSodbo Zh SharapovEvgeny GetmantsevL I MenshikovPeter O FedichevYurii S AulchenkoPublished in: Communications biology (2019)
Aging populations face diminishing quality of life due to increased disease and morbidity. These challenges call for longevity research to focus on understanding the pathways controlling healthspan. We use the data from the UK Biobank (UKB) cohort and observe that the risks of major chronic diseases increased exponentially and double every eight years, i.e., at a rate compatible with the Gompertz mortality law. Assuming that aging drives the acceleration in morbidity rates, we build a risk model to predict the age at the end of healthspan depending on age, gender, and genetic background. Using the sub-population of 300,447 British individuals as a discovery cohort, we identify 12 loci associated with healthspan at the whole-genome significance level. We find strong genetic correlations between healthspan and all-cause mortality, life-history, and lifestyle traits. We thereby conclude that the healthspan offers a promising new way to interrogate the genetics of human longevity.
Keyphrases
- genome wide
- endothelial cells
- dna methylation
- copy number
- induced pluripotent stem cells
- pluripotent stem cells
- metabolic syndrome
- small molecule
- cardiovascular disease
- cardiovascular events
- type diabetes
- gene expression
- high throughput
- genome wide association study
- single cell
- drosophila melanogaster
- risk assessment
- human health
- climate change
- big data
- artificial intelligence